Key result
Microparticles drive vascular dysfunction, prothrombotic signaling, and inflammation in atherothrombosis.
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Cell activation or apoptosis leads to plasma membrane blebbing and microparticle (MP) release in the extracellular space. MPs are submicron membrane vesicles which express a panel of phospholipids and proteins specific of the cells they are derived from. Exposure of negatively charged phospholipids and tissue factor confers a procoagulant potential to MPs. MPs accumulate in the lipid core of the atherosclertotic plaque and is a major determinant of its thrombogenecity. Elevation of plasma MPs levels, particularly those of endothelial origin, reflects cellular injury and is considered now as a surrogate marker of vascular dysfunction. Thus, MPs can be seen as triggers of a vicious circle for they promote prothrombogenic and pro-inflammatory responses as well as cellular dysfunction within the vascular compartment. A better knowledge of MP composition and biological effects as well as the mechanisms leading to their clearance will probably open new therapeutic approaches in the treatment of atherothrombosis.
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Leroyer et al. (2008) conducted a review in Atherothrombosis. Microparticles was evaluated. Microparticles act as surrogate markers of vascular dysfunction and promote prothrombogenic and pro-inflammatory responses in atherothrombosis.
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